ADX71441, a novel oral small molecule positive allosteric modulator, on
track
for Phase 1 clinical testing in the first half of 2013

Addex Therapeutics (SIX: ADXN), a leading
company pioneering allosteric modulation-based drug discovery and
development,
announced today achievement of a positive Proof of Concept for its lead
GABA-B
receptor (GABA-BR) positive allosteric modulator (PAM) compound, ADX71441,
in a
validated pre-clinical model of Charcot-Marie-Tooth 1A (CMT1A). CMT1A is a
rare
(1:5,000) hereditary motor and sensory demyelinating peripheral neuropathy
(also
known as Hereditary Motor and Sensory Neuropathy, HMSN) which is caused by
an
intrachromosomal duplication and consecutive toxic overexpression of the
PMP22
gene on chromosome 17. CMT1A is one of the most common inherited peripheral
nerve-related disorders which is passed down through families in an
autosomal
dominant fashion. CMT1A disease becomes evident in young adulthood and
slowly
progresses with distally pronounced muscle weakness and numbness. Pain can
range
from mild to severe. The disease can be highly debilitating with wheel
chair-boundness and is often accompanied by severe cases of neurological
pain. There
is no known cure for this incapacitating disease.

"We are very excited about the promising results obtained with the Addex
GABA-BR
PAM candidate" said Professor Michael Sereda, of the Max-Planck
Institute of
Experimental Medicine, Göttingen, Germany, in whose laboratories the
study was
performed. "Current CMT1A therapies are primarily symptomatic
such as
physiotherapy and only focus on the manifestations of the disease,
while the
data obtained with the Addex compound seem to suggest that positive
modulation
of GABA-B receptor could lower toxic PMP22 overexpression and potentially
delay
the progression of the disease and offer a unique therapeutic
opportunity for
CMT1A patients".

ADX71441 is a potent, selective, orally available small molecule that is
brain
penetrant and shows good pharmacokinetic properties for once-daily dosing.
Addex
GABA-BR PAM was studied in the transgenic CMT rat model which has 1.6-fold
PMP22
overexpression (mRNA level) and exhibits clinical abnormalities, such as
reduced
nerve conduction velocity and lower grip strength that mimic findings in
CMT1A
patients. Nine week oral therapy of ADX71441 in CMT rats (5 weeks every
other
day at 10 mg/kg followed by 4 weeks at 5 mg/kg every day) down regulated
PMP22
mRNA, reduced the amount of hypo-myelinated axons and increased compound
muscle
action potentials in peripheral nerves when compared to vehicle
treated CMT
rats. It also prevented grip strength loss in CMT rats compared to wild
type
rats.

"These data confirm previous observations obtained using a GABA-BR
agonist and
the GABAB1-/- mice (knock-out mice), which identified the importance of
GABA-BR
in the inhibition of the proliferation and in the reduction of the
synthesis of
specific myelin proteins, in particular PMP22" noted Sonia Poli, VP Non
Clinical
Development at Addex. "These and other data further reinforce the central
role
of GABA-BR in a broad range of important diseases and conditions,
including
spasticity, Fragile X, autism, pain, anxiety, obsessive-compulsive
disorder,
overactive bladder and alcohol binge drinking".

"We are rapidly advancing ADX71441 into clinical development. Phase 1
clinical
testing with this compound is planned for the first half of this year,
initially
for the treatment of spasticity associated with multiple sclerosis (MS)"
said
Graham Dixon, CSO at Addex. "These data are very encouraging as they
indicate
that the compound may also have a therapeutic benefit in treatment of
patients
with this debilitating rare disease."

About CMT1A

CMT1A is a rare hereditary motor and sensory neuropathy (HMSN) which
causes
demyelination of the peripheral nerves with a consequence of
severely and
uniformly reduced nerve conduction velocities and consecutive axonal
loss. The
disease leads to damage or destruction to the myelin sheath covering
around
nerve fibers. Nerves that stimulate movement, the motor nerves, are
most
severely affected. The nerves in the legs are affected first and most
severely.
Similar symptoms may appear in the arms and hands, which may include a
claw-like
hand. The disease is highly invalidating with cases of accompanying
neurological
pain and muscle loss. A combination of lower motor neuron-type motor
deficits
and sensory symptoms are observed: paresis and muscle atrophy develops,
with
areflexia. The chronic nature of the motor neuropathy will result in
foot
deformity, hammertoes, very high-arched feet, loss of lower leg muscle,
which
leads to skinny calves, numbness in the foot or leg, "steppage" gait
(feet hit
the floor hard when walking), foot drop (inability to hold foot
horizontal) and
weakness of the hips, legs, or feet. Involvement of the hands may follow
as the
disease progresses. Signs of sensory system dysfunction are common
(70%) and
include loss of vibration and joint position sense followed by decreased
pain
and temperature sensation. Onset of the disease is between age 5 and 25
years,
with a prevalence of 1 in 5,000. Charcot-Marie-Tooth is one of the most
common
inherited nerve-related disorders passed down through families in an
autosomal
dominant fashion. Charcot-Marie-Tooth disease slowly gets worse. Some
parts of
the body may become numb, and pain can range from mild to severe.
Eventually the
disease may cause disability. There are no known cures for this
debilitating
condition. Duplication of a chromosome 17 fragment harbouring PMP22 (=
CMT1A)
represents 43% of the total CMT cases, whereas the yield of
duplication
detection rises to 70% in CMT1. PMP22 is an essential component of
myelin
expressed in all myelinated fibers in the PNS and is produced by Schwann
cells.
While PMP22 represents only 2-5% of the amount of peripheral myelin
protein in
rodents and humans, it is necessary for stabilizing compact myelin.
However,
PMP22 is not only an essential constituent of myelin, but too much or too
little
of the protein causes neuropathy, possibly by disturbing Schwann cell
growth and
differentiation.

About GABABR

Activation of gamma-aminobutyric acid subtype B (GABA-B) receptor, a
Family C
class of GPCR, is clinically & commercially validated. Generic GABA-B
receptor
agonist, baclofen, is marketed for spasticity and some spinal cord
injuries, and
used for OAB, but is not commonly used due to severe side effects of the
drug
and rapid clearance. Orthosteric GABA-B receptor agonists have also
shown
clinical validation in gastroesophageal reflux disease (GERD). Addex'
GABA-B
receptor PAMs have shown efficacy in multiple preclinical models
including:
CMT1A, OAB, pain, osteoarthritis pain and anxiety.

Addex Therapeutics (www.addextherapeutics.com) discovers and
develops an
emerging class of small molecule drugs, called allosteric modulators, which
have
the potential to be more specific and confer significant therapeutic
advantages
over conventional "orthosteric" small molecule or biological drugs. The
Company
uses its proprietary discovery platform to address receptors and other
proteins
that are recognized as attractive targets for modulation of important
diseases
with unmet medical needs. The Company's two lead products are being
investigated
in Phase 2 clinical testing: dipraglurant (ADX48621, an mGlu5
negative
allosteric modulator or NAM) is being developed by Addex to treat
Parkinson's
disease levodopa-induced dyskinesia (PD-LID); and ADX71149 (mGlu2
positive
allosteric modulator or PAM) is being developed in collaboration with
Janssen
Pharmaceuticals Inc. to treat schizophrenia and anxiety seen in
patients
suffering from major depressive disorder. Addex also is advancing
several
preclinical programs including: GABA-BR PAM for spasticity in MS, OAB and
other
disorders; mGlu4 PAM for Parkinson's, MS, anxiety and other
diseases. In
addition, Addex is applying its proprietary discovery platform to
identify
highly selective and potent allosteric modulators of a number of both
GPCR and
non-GPCR targets that are implicated in diseases of significant unmet
medical
need.

Disclaimer: The foregoing release may contain forward-looking statements
that
can be identified by terminology such as "not approvable",
"continue",
"believes", "believe", "will", "remained open to exploring", "would",
"could",
or similar expressions, or by express or implied discussions regarding
Addex
Therapeutics, formerly known as, Addex Pharmaceuticals, its
business, the
potential approval of its products by regulatory authorities, or
regarding
potential future revenues from such products. Such forward-looking
statements
reflect the current views of Addex Therapeutics regarding future events,
future
economic performance or prospects, and, by their very nature, involve
inherent
risks and uncertainties, both general and specific, whether known or
unknown,
and/or any other factor that may materially differ from the plans,
objectives,
expectations, estimates and intentions expressed or implied in such
forward-looking statements. Such may in particular cause actual results
with allosteric
modulators of mGlu2, mGlu4, mGlu5, GABA-BR or other therapeutic targets
to be
materially different from any future results, performance or
achievements
expressed or implied by such statements. There can be no guarantee
that
allosteric modulators of mGlu2, mGlu4, mGlu5, GABA-BR or other
therapeutics
targets will be approved for sale in any market or by any regulatory
authority.
Nor can there be any guarantee that allosteric modulators of mGlu2,
mGlu4,
mGlu5, GABA-BR or other therapeutic targets will achieve any particular
levels
of revenue (if any) in the future. In particular, management's
expectations
regarding allosteric modulators of mGlu2, mGlu4, mGlu5, GABA-BR or
other
therapeutic targets could be affected by, among other things, unexpected
actions
by our partners, unexpected regulatory actions or delays or
government
regulation generally; unexpected clinical trial results, including
unexpected
new clinical data and unexpected additional analysis of existing clinical
data;
competition in general; government, industry and general public
pricing
pressures; the company's ability to obtain or maintain patent or
other
proprietary intellectual property protection. Should one or more of these
risks
or uncertainties materialize, or should underlying assumptions prove
incorrect,
actual results may vary materially from those anticipated, believed,
estimated
or expected. Addex Therapeutics is providing the information in this
press
release as of this date and does not undertake any obligation to
update any
forward-looking statements contained in this press release as a result
of new
information, future events or otherwise, except as may be required by
applicable
laws.

This announcement is distributed by Thomson Reuters on behalf of
Thomson Reuters clients. The owner of this announcement warrants that:

(i) the releases contained herein are protected by copyright and
other applicable laws; and

(ii) they are solely responsible for the content, accuracy and
originality of the information contained therein.

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